Niflumic acid
Based on 6 publication(s) in Google Scholar
Niflumic acid is a calcium-activated chloride channel blocker and COX-2 inhibitor with the IC50 value of 100 nM. Niflumic acid induces apoptosis through caspase-8/Bid/Bax pathway in lung cancer cells. Niflumic acide exhibits anti-tumor activity by affecting the expression of ERK1/2 and the activity of MMP2 and MMP9. Niflumic acid has orally bioactivity. Niflumic acid acts on rheumatoid arthritis.
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- Purity : 99.61%
- CAS No.: 4394-00-7
- 화학식: C13H9F3N2O2
- 분자량:282.22
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보관:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year
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Biological Activity
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Chemical Information
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용액&용해도
- Protocol
- 순도&문서
- References
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Help & FAQs
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Niflumic acid (Standard)Chloride Channel/COX Inhibitor -
HY-103370
TalniflumateCaCC Blocker
Publications Citing Use of MedChemExpress (MCE) Niflumic acid
More- Sci Adv. 2026 Mar 6;12(10):eadw0891. [Abstract]
- J Ethnopharmacol. 2026 Mar 25:359:121101. [Abstract]
- Biochem Pharmacol. 2025 Feb:232:116720. [Abstract]
- Cell Calcium. 2026 May 23:136:103155. [Abstract]
- Comput Struct Biotechnol J. 2023 Feb 24:21:1907-1920. [Abstract]
- Physiol Rep. 2026 Jun;14(11):e70975. [Abstract]
Biological Activity
제품 설명
IC50 & Target
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COX-2 100 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| Bone marrow cell | EC50 |
>20 μM
Compound: Niflumic acid
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Induction of bone marrow cell differentiation isolated from ER-HOXA9 fusion protein expressed mouse harboring GFP-lysozyme assessed as upregulation of CD11b/MAC1 after 4 days by flow cytometry
Induction of bone marrow cell differentiation isolated from ER-HOXA9 fusion protein expressed mouse harboring GFP-lysozyme assessed as upregulation of CD11b/MAC1 after 4 days by flow cytometry
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[PMID: 27994748] |
| CHO | EC50 |
30.8 μM
Compound: 8
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Agonist activity at C-terminal beta-galactosidase tagged human recombinant GPR35 expressed in CHO cells after 90 mins by beta-arrestin recruitment assay
Agonist activity at C-terminal beta-galactosidase tagged human recombinant GPR35 expressed in CHO cells after 90 mins by beta-arrestin recruitment assay
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[PMID: 23888932] |
| HEK293 | IC50 |
13 μM
Compound: Niflumic acid
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Inhibition of human recombinant UGT1A1 expressed in HEK293 cells assessed as reduction in estradiol 3-glucuronidation by LC-MS/MS method
Inhibition of human recombinant UGT1A1 expressed in HEK293 cells assessed as reduction in estradiol 3-glucuronidation by LC-MS/MS method
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[PMID: 21030469] |
| HEK293 | IC50 |
53 μM
Compound: Niflumic acid
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Inhibition of human recombinant UGT1A1 expressed in HEK293 cells assessed as reduction in bilirubin glucuronidation by LC-MS/MS method
Inhibition of human recombinant UGT1A1 expressed in HEK293 cells assessed as reduction in bilirubin glucuronidation by LC-MS/MS method
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[PMID: 21030469] |
| HEK-293T | EC50 |
15 μM
Compound: 8
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Agonist activity at human GPR35 expressed in HEK293T cells at 5 uM by EYPF-based beta-arrestin-2 luciferase reporter gene assay
Agonist activity at human GPR35 expressed in HEK293T cells at 5 uM by EYPF-based beta-arrestin-2 luciferase reporter gene assay
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[PMID: 23888932] |
| HT-29 | EC50 |
1.15 μM
Compound: Niflumic acid
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Agonist activity at GPR35 receptor in human HT-29 cells after 10 mins by dynamic mass redistribution assay
Agonist activity at GPR35 receptor in human HT-29 cells after 10 mins by dynamic mass redistribution assay
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[PMID: 24900447] |
| HT-29 | IC50 |
1.28 μM
Compound: Niflumic acid
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Desensitization of GPR35 receptor in human HT-29 cells assessed as inhibition of zaprinast-induced dynamic mass redistribution after 10 mins
Desensitization of GPR35 receptor in human HT-29 cells assessed as inhibition of zaprinast-induced dynamic mass redistribution after 10 mins
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[PMID: 24900447] |
| THP-1 | EC50 |
>20 μM
Compound: Niflumic acid
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Induction of human THP1 cell differentiation after 4 days by flow cytometry
Induction of human THP1 cell differentiation after 4 days by flow cytometry
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[PMID: 27994748] |
| U2OS | EC50 |
40.2 μM
Compound: Niflumic acid
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Agonist activity at GPR35 receptor in human U2OS cells coexpressing Gal4-VP16-TEV assessed as beta arrestin translocation after 5 hrs by beta lactamase reporter gene assay
Agonist activity at GPR35 receptor in human U2OS cells coexpressing Gal4-VP16-TEV assessed as beta arrestin translocation after 5 hrs by beta lactamase reporter gene assay
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[PMID: 24900447] |
| U-937 | EC50 |
>20 μM
Compound: Niflumic acid
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Induction of human U937 cell differentiation after 4 days by flow cytometry
Induction of human U937 cell differentiation after 4 days by flow cytometry
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[PMID: 27994748] |
In Vitro
Niflumic acid (100 and 200 μM; 48 h) combined with Ciglitazone (HY-W011220) exerts cytotoxic effect against A549, H460, and H1299 cells[5].
Niflumic acid (0-300 μM; 36 h) combined with Ciglitazone induces apoptosis in A549, H460, and H1299 cells[5].
Niflumic acid (100 μM; 30 h) combined with Ciglitazone induces activates caspase-8/Bid/Bax pathway in lung cancer cells[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:A549, H460, and H1299 cells
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Concentration:0 μM, 100 μM,200 μM, 300 μM
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Incubation Time:48 h
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Result:Showed a marked synergistic decrease in cell viability with Ciglitazone.
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Cell Line:A549, H460, and H1299 cells
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Concentration:100 μM, 200 μM
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Incubation Time:48 h
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Result:Showed a marked synergistic increase apoptosis with Ciglitazone.
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Cell Line:A549, H460, and H1299 cells
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Concentration:100 μM
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Incubation Time:30 h
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Result:Showed a marked synergistic increase of proteins level of caspase-8, Bid, and Bax with Ciglitazone.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Pig with asthma [8]
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Dosage:30 mg/kg
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Administration:Inhalation
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Result:Showed significantly inhibiting the decrease in mucus area.
Chemical Information
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CAS No. 4394-00-7
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Appearance Solid
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분자량 282.22
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화학식 C13H9F3N2O2
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Color White to yellow
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SMILES
O=C(C1=CC=CN=C1NC2=CC=CC(C(F)(F)F)=C2)O
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Publications (6)
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Journal Impact Factor
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Most Recent
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Sci Adv
A worm-like nucleic acid nanostructure for gene delivery and endosomal escape via ClC3 ion exchanger. [Abstract]2026 Mar 6;12(10):eadw0891. PMID: 41790895 -
J Ethnopharmacol
Shenling Baizhu powder alleviates pyrotinib-induced diarrhea via CFTR-activated chloride secretion. [Abstract]2026 Mar 25:359:121101. PMID: 41461327 -
Biochem Pharmacol
E3 ubiquitin ligase ITCH-mediated proteasomal degradation of WBP2 sensitizes breast cancer cells to chemotherapy through restraining AMOTL2/c-JUN axis. [Abstract]2025 Feb:232:116720. PMID: 39709035 -
Cell Calcium
Drug repurposing DMSO from an old solvent to a new candidate for the treatment of colitis and sepsis in male mice. [Abstract]2026 May 23:136:103155. PMID: 42235215 -
Comput Struct Biotechnol J
Network Proximity-based computational pipeline identifies drug candidates for different pathological stages of Alzheimer's disease. [Abstract]2023 Feb 24:21:1907-1920. PMID: 36936813 -
Physiol Rep
Monosodium glutamate-mediated Ca2+-dependent intestinal epithelial ion transports in health and IBS-D in male mice. [Abstract]2026 Jun;14(11):e70975. PMID: 42281391
용액&용해도
In Vitro:
DMSO : ≥ 100 mg/mL (354.33 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : < 0.1 mg/mL (insoluble)
* "≥" means soluble, but saturation unknown.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.5 mg/mL (8.86 mM); Clear solution
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocol
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Collagen-Induced Arthritis
Collagen-induced arthritis (CIA) is an autoimmune murine model of rheumatoid arthritis in which immunization with type II collagen (CII) emulsified in an adjuvant induces a T cell- and autoantibody-driven inflammatory arthritis characterized by synovial hyperplasia, immune cell infiltration, and joint destruction. The model typically relies on genetically susceptible mouse strains (e. g. , DBA/1) and reproduces key features of human rheumatoid arthritis, including anti-collagen immune responses and progressive joint inflammation. Disease onset generally occurs within ~3-4 weeks after immunization, depending on antigen/adjuvant combinations and protocol variation. The immunopathology is driven by adaptive immune activation against CII, leading to systemic and local joint inflammation mediated by pro-inflammatory cytokines and effector immune cells, making CIA a standard preclinical platform for evaluating immunomodulatory and anti-arthritic interventions.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
순도&문서
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Data Sheet (281 KB)
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SDS (480 KB)
- English - EN (480 KB)
- Français - FR (480 KB)
- Deutsch - DE (480 KB)
- Norwegian - NO (480 KB)
- Español - ES (480 KB)
- Swedish - SV (480 KB)
- Italian - IT (480 KB)
- Korean - KR (480 KB)
- Portuguese - PT (480 KB)
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Handling Instructions (2659 KB)
References
[1]. Criddle, D.N., et al., Inhibitory action of niflumic acid on noradrenaline- and 5-hydroxytryptamine-induced pressor responses in the isolated mesenteric vascular bed of the rat. Br J Pharmacol, 1997. 120(5): p. 813-8. [Content Brief]
[2]. Jabeen, T., et al., Non-steroidal anti-inflammatory drugs as potent inhibitors of phospholipase A2: structure of the complex of phospholipase A2 with niflumic acid at 2.5 Angstroms resolution. Acta Crystallogr D Biol Crystallogr, 2005. 61(Pt 12): p. 1579-86. [Content Brief]
[3]. Picollo, A., et al., Mechanism of interaction of niflumic acid with heterologously expressed kidney CLC-K chloride channels. J Membr Biol, 2007. 216(2-3): p. 73-82. [Content Brief]
[4]. Yuliya V Kucherenko, et al. Niflumic Acid Affects Store-Operated Ca2+-Permeable (SOC) and Ca2+-Dependent K+ and Cl2 Ion Channels and Induces Apoptosis in K562 Cells. J Membr Biol. 2014 Jul;247(7):627-38. [Content Brief]
[5]. Byeong Mo Kim, et al. Combined treatment with the Cox-2 inhibitor niflumic acid and PPARc ligand ciglitazone induces ER stress/caspase-8-mediated apoptosis in human lung cancer cells. Cancer Lett. 2011 Jan 28;300(2):134-44. [Content Brief]
[6]. Shengqun Luo , et al. Niflumic acid exhibits anti-tumor activity in nasopharyngeal carcinoma cells through affecting the expression of ERK1/2 and the activity of MMP2 and MMP9. Int J Clin Exp Pathol [Content Brief]
[8]. Mitsuko Kondo , et al. Niflumic Acid Inhibits Goblet Cell Degranulation in a Guinea Pig Asthma Model. Allergol Int. 2012 Mar;61(1):133-42. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 3.5433 mL | 17.7167 mL | 35.4333 mL | 88.5834 mL |
| 5 mM | 0.7087 mL | 3.5433 mL | 7.0867 mL | 17.7167 mL | |
| 10 mM | 0.3543 mL | 1.7717 mL | 3.5433 mL | 8.8583 mL | |
| 15 mM | 0.2362 mL | 1.1811 mL | 2.3622 mL | 5.9056 mL | |
| 20 mM | 0.1772 mL | 0.8858 mL | 1.7717 mL | 4.4292 mL | |
| 25 mM | 0.1417 mL | 0.7087 mL | 1.4173 mL | 3.5433 mL | |
| 30 mM | 0.1181 mL | 0.5906 mL | 1.1811 mL | 2.9528 mL | |
| 40 mM | 0.0886 mL | 0.4429 mL | 0.8858 mL | 2.2146 mL | |
| 50 mM | 0.0709 mL | 0.3543 mL | 0.7087 mL | 1.7717 mL | |
| 60 mM | 0.0591 mL | 0.2953 mL | 0.5906 mL | 1.4764 mL | |
| 80 mM | 0.0443 mL | 0.2215 mL | 0.4429 mL | 1.1073 mL | |
| 100 mM | 0.0354 mL | 0.1772 mL | 0.3543 mL | 0.8858 mL |
Niflumic acid Related Classifications
HY-B0493 Related Classifications
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